Acute Adrenal Insufficiency

Causes:

➧ Usually presents as an acute process in a patient with underlying chronic adrenal insufficiency

➧ Causes of Primary adrenal insufficiency:

   - Auto-immune

   - TB of adrenals

   - Metastatic malignancy to adrenals

➧ Causes of Secondary or Tertiary adrenal insufficiency

   - Pituitary or hypothalamic disease

➧ Acute destruction of the adrenals can occur with bleeding in the adrenals:

   - Sepsis

   - Disseminated intravascular coagulopathy (DIC)

   - Complication of anticoagulant therapy

Precipitating factors:

➧ Omission of medication

➧ Precipitating illness:

   - Severe infection

   - Myocardial infarction

   - Cerebro-vascular accident (CVA)

   - Surgery without adrenal support

   - Severe trauma

➧ Withdrawal of steroid therapy in a patient on long-term steroid therapy (Adrenal atrophy)

➧ Administration of drugs impairing adrenal hormone synthesis e.g. Ketoconazole

➧ Using drugs that increase steroid metabolism e.g. Phenytoin and Rifampicin

Clinical picture:

➧ Nausea and vomiting

➧ Hyperpyrexia

➧ Abdominal pain

➧ Dehydration

➧ Hypotension and shock

Clues to underlying Chronic Adrenal Insufficiency:

➧ Pigmentation in unexposed areas of the skin:

   - Creases of hands

   - Buccal mucosa

   - Scars

➧ Consider adrenal insufficiency if hypotension does not respond to pressors

Laboratory diagnosis:

➧ Hyponatremia and hyperkalemia (Hyponatremia might be obscured by dehydration).

➧ Random cortisol is not helpful unless it is very low (less than 5 mg/L) during a period of great stress.

➧ ACTH (Cosyntropin) stimulation test:

- Failure of cortisol to rise above 552 nmol/L 30 min after administration of 0.25 mg of synthetic ACTH IV

➧ Basal ACTH will be raised in primary adrenal insufficiency but not in secondary.

➧ CT of the abdomen will reveal enlargement of adrenals in patients with adrenal hemorrhage, active TB, or metastatic malignancy.

Management of Acute Adrenal Insufficiency:

➧ Hydrocortisone: 200 mg IV stat then 100 mg/8 h. for 24 h

-Taper slowly over the next 72 h.

-When oral feeds are tolerated change to oral replacement therapy.

-Overlap the first oral and last IV doses.

➧ Dexamethasone: 10 mg/6 h. IV

➧ Fludrocortisone: 0.05-0.3 mg/d. (if hydrocortisone less than 100 mg/d).

-Patients with primary adrenal insufficiency may require mineralocorticoid therapy (fludrocortisone) when shifted to oral therapy.

➧ 5% dextrose: IV for hypoglycemia

➧ Normal saline: IV for volume expansion

➧ Treat precipitating diseases

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Pituitary Apoplexy

Clinical Setting:

➧ Hemorrhagic infarction of a pituitary adenoma/tumor.

➧ Sudden crisis in a patient with a known or previously unknown pituitary tumor.

➧ It may occur in a normal gland during and after childbirth, with head trauma, or in a patient on anticoagulation therapy. 

➧ Sheehan’s Syndrome:

-Refers to pituitary apoplexy of the non-tumorous gland. It is due to the postpartum arterial spasm of arterioles supplying the anterior pituitary and its stalk.

Clinical Picture:

➧ Severe headache and visual disturbance

➧ Bitemporal hemianopia (Figure 1)

➧ CN III palsy

➧ Meningeal symptoms with neck stiffness

➧ Symptoms of secondary acute adrenal insufficiency:

-Nausea, vomiting, hypotension, and collapse

Figure 1: Bitemporal Hemianopia

Diagnosis:

➧ CT/MRI scan of head and pituitary

➧ Hormonal studies only of academic interest

➧ Assessment of pituitary function after the acute stage has settled

Management:

a) Hormonal:

➧ Dexamethasone: 4 mg/12 h.

-Glucocorticoid support and relief of cerebral edema.

b) Neurosurgical:

➧ Transsphenoidal pituitary decompression

-After the acute episode the patient must be evaluated for multiple pituitary deficiencies.

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Pheochromocytoma Crisis

Causes:

➧ The action of unopposed high circulating levels of catecholamines

- α - receptors: Pressor response

- β - receptors: positive ino- and chrono-topic

Precipitating factors:

➧ Spontaneous

➧ Hemorrhage into pheochromocytoma

➧ Exercise

➧ Pressure on the abdomen

➧ Urination

➧ Drugs: glucagon, naloxone, metoclopramide, ACTH, cytotoxics, tricyclic antidepressants

Clinical picture:

➧ History of poorly controlled Hypertension or accelerated Hypertension.

➧ Hypertension, palpitations, sweating, pallor, pounding headache, anxiety, tremulousness, pulmonary edema, feeling of impending death, hyperhidrosis, nausea and vomiting, abdominal pain, paralytic ileus, hyperglycemia, hypertensive encephalopathy, myocardial infarction, and stroke.

➧ Attacks build up over a few minutes and fade gradually over 15 min or can be more sustained (60 min).

➧ Signs of end-organ damage (Figure 1)

Figure 1: Hypertensive Retinopathy - Grade IV

Biochemical Diagnosis:

➧ 24 h. urine collection for free catecholamines and metanephrines.

Management of Pheochromocytoma Crisis:

-Do not wait for biochemical confirmation of the diagnosis.

-Be aware of postural hypotension.

-Avoid histamine-releasing drugs.

-Surgical resection treatment of choice.

α-adrenergic blockers:

-Treatment with a-antagonists should precede β-antagonist treatment with 48 h. to avoid exacerbation of the crisis.

➧ Phentolamine: (short-acting) 2-5 mg IV repeated/5 min.

➧ Phenoxybenzamine: 1st choice because it’s irreversible and long-acting

10 mg/12h., then 20-40 mg/8 h.

➧ Prazosin, Terazosin & Doxazosin: are selective α1-blockers. Preferable for long term Rx due to favorable S/E

β-blockers:

-Control tachycardia.

-After adequate α-adrenergic blockage to prevent unopposed hypertension.

➧ Non selective b- antagonist: Propranolol: 1-2 mg/5-10 min. 30-60 mg/d. oral.

➧ Esmolol: 500 µg/kg/min. for 1 min., then 100-300 µg/kg/min.

➧ Metoprolol

➧ Labetalol: α and β blocker.

Catecholamine synthesis inhibitors:

➧ Metyrosine

-Inhibit catecholamine synthesis.

-Used when alpha &beta blockers are ineffective or poorly tolerated.

-Combined for difficult resections.

Calcium channel blockers:

-Inhibit norepinephrine mediated calcium transport.

Acute hypertensive crisis (pre/intra-op):

➧ Nitroprusside

➧ Phentolamine

➧ Nicardipine

Surgery and Post-operative care:

➧ Experienced surgeon/anesthetist team.

➧ Last α & β doses on the day of surgery.

➧ Avoid fentanyl, ketamine, morphine, atropine, halothane, and desflurane during surgery.

➧ Treat hypotension post resection with fluids and intermittent doses of vasopressors.

➧ 24 h. urine metanephrine & catecholamine level 1-2 wks post-surgery and annually for life.

➧ Lifelong glucocorticoid and mineralocorticoid therapy for bilateral adrenalectomy.

➧ Radiotherapy, cryoablation, and combination chemotherapy should be considered for malignant pheochromocytoma.

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Burn Fluid Resuscitation Formulas

1-Harkins formula (1942)

Initial 24 hours:

➧ 1000 ml plasma/10% burn Used in patients with ≥ 10% burn.

2-Body weight burn budget (1947)

Initial 24 hours:

➧ Ringer's lactate (RL) solution 1-4 L + 1200ml NS + 7.5% body weight colloid + 1.5-5 L D5W.

Next 24 hours: 

➧ RL 1-4 L + 1200ml NS + 2.5%body weight colloid + 1.5-5 L D5W.

3-Evans formula (1952)

Initial 24 hours:

➧ 0.9% saline at 1 ml/kg/% burn + colloids at 1 ml/kg/% burn + 2000 ml G5W.

Next 24 hours:

➧ 0.9% saline at 0.5 ml/kg/% burn + colloids at 0.5 ml/kg/% burn + 2000 ml G5W.

4-Brooke formula (1953)

Initial 24 hours:

➧ RL solution 1.5 ml/kg/% burn + Colloids 0.5 ml/kg/% burn + 2000 ml G5W.

Next 24 hours:

➧ RL 0.5 ml/kg/% burn + Colloids 0.25 ml/kg/% burn + 2000 ml G5W.

5-Modified Brooke formula (1979)

Initial 24 hours:

➧ RL solution 2 ml/kg/% burn (for adults).

➧ RL solution 3 ml/kg/% burn (for children).

Next 24 hours:

➧ Colloids at 0.3-0.5 ml/kg/% burn.

➧ G5W to maintain good urinary output.

N.B. Pediatric supplementation for children less than 20 kg: RL at calculated maintenance.

6-Parkland formula (Baxter and Shires) (1974)

Initial 24 hours:

➧ RL solution 4 ml/kg/% burn (for adults).

➧ RL solution 3 ml/kg/% burn (for children).

Next 24 hours:

➧ Colloids are given as 20-60% of calculated plasma volume. 

➧ G5W is added in amounts required to maintain a urinary output of 0.5-1 ml/kg/h (in adults) & 1 ml/kg/h (in children).

7-Modified Parkland formula

Initial 24 hours:

➧ RL 4 ml/kg/% burn (for adults).

Next 24 hours:

➧ 5% albumin 0.3-1 ml/kg/% burn/16 per h.

8-Consensus (by the American Burn Association)

Initial 24 hours:

➧ RL solution 2-4 ml/kg/% burn.

Next 24 hours:

➧ Colloids at 0.3-0.5 ml/kg/% burn. 

➧ G5W is added in the amounts required to maintain good urinary output.

9-Mount Vernon (Muir and Barclay) formula

➧ Used in >15% burn (in adults) or >10% burn (in children).

➧ 1 ml/kg/% burn, Type of fluid: 50% crystalloids + 50% colloids (5% albumin).

➧ This volume is given in each of the following 6 periods: (0-4, 4-8, 8-12, 12-18, 18-24, 24-36h.)

10-Hypertonic saline formula

➧ NS containing: 250 mEq Na⁺ (0.6 ml/kg/% burn) + 1/3 isotonic salt solution orally up to 3500 ml.

11-Monafo (Hypertonic saline) formula (1984)

Initial 24 hours:

➧ NS containing: 250 mEq Na⁺ + 150 mEq lactate⁻ + 100 mEq Cl⁻. The amount is adjusted to maintain a urine output of 30 ml/h.

Next 24 hours:

➧ 1/3 normal saline according to urinary output.

12-Modified hypertonic formula (Metro Health Medical Center)

Initial 24 hours:

➧ RL + 50 mEq NaHCO₃ (180 mEq Na/L) RL 4 ml/kg/% burn titrated to urine output.

Next 24 hours:

➧ ½ NS + One unit FFP/L ½ NS + G5W to prevent hypoglycemia.

13-Slater formula

➧ (RL 2000ml + FFP 75 ml/kg)/24 h.

Formulas developed for children:

1-Shriner's Cincinnati formula

Initial 24 hours:

For older children:

➧ RL solution 4 ml/kg/% of burned tissue (burn-related losses) + 1500 ml/m² total BSA (maintenance fluid) (1/2 of total volume over 8 h, rest of the total volume during the following 16 h).

For younger children:

➧ 4 ml/kg/% of burned tissue (burn-related losses) + 1500 ml/m² total BSA (maintenance fluid).

➧ RL solution + 50 mEq NaHCO₃ in the first 8 h.

➧ RL solution in the second 8 h.

➧ 5% albumin in RL solution in the third 8 h.

2-Galveston formula

➧ Every 1000 ml of the solution consists of 50 ml of 25% albumin added to 950 ml of 5% D5W in the RL solution.

Initial 24 hours:

➧ 5000 ml/m² of burned tissue (burn-related losses) + 2000 ml/m² total BSA (maintenance fluid) (1/2 of total volume over 8 h, rest of the total volume during the following 16 h).

Next 24 hours:

➧ 3750 ml/m² of burned tissue (burn-related losses) + 1500 ml/m² total BSA (maintenance fluid). 

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Ropivacaine (Naropin®)

➧ Ropivacaine is a long-acting amide local anesthetic (LA) drug. The name ropivacaine refers to both the racemic mixture and the marketed S-enantiomer.

➧ It produces effects similar to other LAs via reversible inhibition of sodium ion influx in nerve fibers.

Advantages:

➧ Ropivacaine is less lipophilic than bupivacaine and is less likely to penetrate large myelinated motor fibers, resulting in a relatively reduced motor blockade. Thus, ropivacaine has a greater degree of motor-sensory differentiation, which could be useful when the motor blockade is undesirable. 

➧ The reduced lipophilicity is also associated with decreased potential for central nervous system toxicity and cardiotoxicity.

Uses:

1-Epidural anesthesia 

2-Peripheral nerve block 

3-Postoperative pain management 

4-Intrathecal hyperbaric solution of ropivacaine was tried and found to be less potent than bupivacaine and resulted in a faster onset and recovery from the blocks. Hyperbaric ropivacaine solutions are not commercially available.

Contraindications:

1-Intravenous regional anesthesia (IVRA): However, recent data suggested that ropivacaine (1.2-1.8 mg/kg in 40 ml) can be used, because it has less cardiovascular and central nervous system toxicity than racemic bupivacaine. 

2-Intra-articular infusion: Ropivacaine is toxic to cartilage and its intra-articular infusion can lead to Postarthroscopic glenohumeral chondrolysis.

Adverse effects:

a) CNS effects: occur at lower blood plasma concentrations; CNS excitation followed by depression. 

-CNS excitation: nervousness, tingling around the mouth, tinnitus, tremor, dizziness, blurred vision, seizures. 

-CNS depression: drowsiness, loss of consciousness, respiratory depression, and apnea. 

b) Cardiovascular effects: occurs at higher blood plasma concentrations. 

-Hypotension, bradycardia, arrhythmias, and/or cardiac arrest – some of which may be due to hypoxemia secondary to respiratory depression.

Treatment of overdose:

➧ As for bupivacaine, Intralipid, a commonly available intravenous lipid emulsion, can be effective in treating severe cardiotoxicity secondary to local anesthetic overdose in animal experiments and in humans in a process called lipid rescue.

Read more ☛ LA Toxicity

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Down's Syndrome

Anesthetic Management of Down's Syndrome

➧ This well-known syndrome, with characteristic morphological features and mental retardation, results from the chromosomal abnormality, trisomy 21.

➧ Anesthetic risk is increased in these children. Indeed, the mortality is increased at any stage of life, but improved medical and nursing care means that many more individuals are surviving into adulthood and may present for surgery.

➧ Between 60 and 70% of patients now survive beyond 10 years of age.

Preoperative abnormalities:

1. Cardiac abnormalities: occur in 50–60% of patients and are usually responsible for the initial mortality in infancy. The commonest lesions are septal defects, Fallot’s tetralogy, and patent ductus arteriosus. In adults, there is an increased risk of mitral valve prolapse and mitral and aortic valve regurgitation.

2. Immune system defect: results in an increased incidence of infection. Granulocyte abnormalities decreased adrenal responses, and defects in cell-mediated immunity have all been identified. There is an increased incidence of lymphomas and leukemias.

3. Skeletal abnormalities: atlantoaxial instability was recognized as being a problem, at a time when these children were encouraged to participate in gymnastics. Down’s children may have C1–C2 articulation abnormalities, subluxation, and odontoid peg abnormalities. It may occur in association with either medical procedures or physical activity. The cause of instability may be due to: poor muscle tone, ligamentous laxity, and abnormal development of the odontoid peg.

4. Biochemical abnormalities: involve the metabolism of serotonin, catecholamines, and amino acids.

5. Thyroid hypofunction: is common in both adults and children, although hyperthyroidism can sometimes occur. A child with Down’s syndrome had a thyrotoxic crisis that mimicked malignant hyperthermia.

6. Sleep-induced ventilatory dysfunction: has been reported.

7. Institutionalized Down’s patients have an increased incidence of hepatitis B antigen.

8. Autonomic dysfunction: in particular increased sympathetic function and decreased vagal activity, result from brainstem abnormalities.

Anesthetic problems:

1. Cervical spine abnormalities: increase the risk of dislocation of certain cervical vertebrae on intubation, or when the patient is paralyzed with muscle relaxants with risk of atlantoaxial subluxation and spinal cord compression. Cervical spine screening has to be carried out, and precautions taken during intubation. 

2. The larynx is often underdeveloped and smaller tracheal tube size is required than would be anticipated for the age of the patient. The adult larynx may only accept a size 6-mm tube.

3. Airway and intubation difficulties sometimes occur, from a combination of anatomical features. These include a large tongue, a small mandible and maxilla, a narrow nasopharynx, and irregular teeth. Even in the absence of teeth, intubation is made more difficult by excessive pharyngeal tissue.

4. Postoperative stridor after prolonged nasal intubation. Congenital subglottic stenosis occurs occasionally.

5. Obstructive sleep apnea is common in Down’s syndrome. Compared with normal children they had an increased incidence of stridor and chest wall recession, lower baseline oxygen saturations, and a greater number of episodes of desaturation to 90% or less. Chronic episodes of hypoxia and hypercarbia may lead to pulmonary hypertension and congestive heart failure. Airway patency depends upon both the anatomical structure of the upper respiratory tract and the normal functioning of the pharyngeal muscles. Abnormalities of either or both may occur.

6. Upper airway obstruction, because it has multiple causes, is not necessarily resolved with surgical treatment. Young patients with more severe symptoms often had multiple sites of obstruction and a high incidence of cardiac disease.

7. Problems of the associated cardiac disease, which in later life may lead to pulmonary hypertension.

8. A high incidence of atelectasis and pulmonary edema after surgery for congenital heart disease. Those with Down’s syndrome and ventricular septal defects were predisposed to pulmonary vascular obstruction.

9. Posterior arthrodesis of the upper cervical spine carries a high complication rate. Problems included infection and wound dehiscence, instability at a lower level, neurological sequelae, and postoperative death.

Management:

1. Lateral cervical X-rays are required, in full flexion and extension positions, to detect atlantoaxial instability. This may show as an increase in the distance between the posterior surface of the anterior arch of the atlas, and the anterior surface of the odontoid process. Patients with an atlanto-odontoid interval of 4.5–6.0 mm were asymptomatic, but those in whom the distance exceeded 7 mm had neurological signs. If instability is present, great care should be taken to immobilize the neck during intubation and muscle relaxation. These changes do not appear to progress with time. 

2. If a significant cardiac disease is present, management must be appropriate to the lesion, and endocarditis prophylaxis is given as recommended.

3. A tracheal tube should be used that is 1–2 sizes smaller than would be expected from the patient’s age.

4. If prolonged nasotracheal intubation is required, steroids should be given before extubation. The child should receive humidification and be observed carefully for signs of stridor.

5. Close observation is required in the perioperative period, to detect episodes of obstructive apnea. A pulse oximeter is useful.

6. Loss of locomotor skills or disturbances of gait after surgery or acute trauma should alert staff to the possibility of subluxation and cord compression. In the event of this, an urgent neurological opinion should be sought. However, in the absence of neurological signs, non-operative management has been advised, because of the high complication rate after surgery.

7. In patients with adenotonsillar hypertrophy, surgery may improve obstruction. However, close monitoring and oxygen therapy are important for the first postoperative night.

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Propofol Related Infusion Syndrome (PRIS)

➧ It is a rare syndrome that affects patients undergoing long-term treatment with high doses of the anesthetic and sedative drug propofol. 

➧ It is associated with high doses and long-term use of propofol (>4 mg/kg/hr for more than 24 hours). It occurs more commonly in children, and critically ill patients receiving catecholamines and glucocorticoids are at high risk.

Clinical Picture:

➧ Arrhythmias 

➧ Progressive Myocardial Failure 

➧ Cardiovascular Collapse 

➧ Lipemia 

➧ Hypertriglyceridemia 

➧ Acute Renal Failure 

➧ Rhabdomyolysis 

➧ Metabolic acidosis 

➧ Hyperkalemia 

➧ Hepatomegaly 

➧ Green urine (phenol metabolites), (Figure 1) 

➧ It is often fatal 

Figure 1: Green Urine

Laboratory Results:

➧ Elevated serum lactate 

➧ Elevated CPK 

➧ Myoglobinuria 

➧ Hyperkalemia 

➧ Hypertriglyceridemia

ECG changes:

➧ ST elevation in precordial leads V1 to V3

Predisposing factors for developing PRIS:

➧ Propofol dose >4 mg/kg/h 

➧ Propofol infusion >48 h 

➧ Presence of “triggering factor” (i.e. catecholamine infusion or corticosteroids) 

➧ Inadequate delivery of carbohydrate 

➧ Critical Illness 

➧ Severe Cerebral Injury 

➧ Sepsis 

➧ Pancreatitis 

➧ Trauma

Prevention:

➧ Avoid high propofol doses and minimize the duration of infusion in high-risk patients 

➧ Avoid lipid overload by assessing all sources of fat calories (e.g., parenteral nutrition, enteral nutrition). 

➧ Monitoring of serum triglycerides in any patient receiving propofol in doses >4 mg/kg/h or >48 is highly recommended. 

➧ Assure adequate provision of carbohydrates. 

➧ Depletion of carbohydrate stores can promote mobilization of fat stores and increase lipid metabolism. This, in turn, increases circulating fatty acid load and may predispose patients to PRIS. 

➧ Theoretically, it is, therefore, possible that early adequate carbohydrate intake may prevent PRIS by preventing the switch to fat metabolism. 

➧ There is some suggestion that providing a carbohydrate intake of 6–8 mg/kg/min. can suppress fat metabolism and thus prevent PRIS.

Treatment: (Supportive) 

➧ Early recognition of the syndrome and discontinuation of the propofol infusion reduces morbidity and mortality. 

➧ Once a patient presents with symptoms compatible with PRIS, propofol infusion should be discontinued promptly and an alternative sedative agent should be initiated. 

➧ Cardiovascular support by the combination of vasopressors and inotropes. 

➧ Cardiac pacing should be considered. 

➧ Hemodialysis or hemofiltration to decrease the plasma concentrations of circulating metabolic acids and lipids. 

➧ Extracorporeal membrane oxygenation (ECMO) for combined respiratory and circulatory support. 

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Central Anticholinergic Syndrome

➧ Many of the drugs used in anesthesia and intensive care may cause blockage of the central cholinergic neurotransmission.

➧ Acetylcholine is of significance in the modulation of the interaction among most other central transmitters.

Causes:

1- Overdose of anticholinergic drugs: e.g. Atropine, scopolamine, glycopyrrolate

2- Overdose of drugs that possess an anticholinergic activity:

e.g. Antipsychotics, tricyclic antidepressants, antiparkinsonian drugs

3- It May be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine.

Clinical Picture:

➧ The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical to the central symptoms of atropine intoxication.

➧ This behavior consists of agitation including seizures, restlessness, hallucinations, disorientation, or signs of depression such as stupor, coma, and respiratory depression.

Systemic:

➧ Tachycardia: Increased heart rate

➧ Ataxia: loss of coordination 

➧ Dry, sore throat, xerostomia, or dry mouth with a possible acceleration of dental caries 

➧ Cessation of perspiration → Increased body temperature 

➧ Mydriasis: Pupil dilation; consequent sensitivity to bright light (photophobia) 

➧ Cycloplegia: Loss of accommodation (loss of focusing ability, blurred vision) 

➧ Diplopia: Double-vision 

➧ Increased intraocular pressure; dangerous for people with narrow-angle glaucoma

➧ Urinary retention, Diminished bowel movement, and sometimes ileus

➧ Shaking

Central nervous system:

Resemble those associated with delirium, and may include:

➧ Mental confusion (brain fog), Disorientation, Agitation, Irritability, Unusual sensitivity to sudden sounds 

➧ Euphoria or dysphoria 

➧ Memory problems, Inability to concentrate

➧ Illogical thinking, Wandering thoughts; inability to sustain a train of thought 

➧ Incoherent speech 

➧ Respiratory depression 

➧ Wakeful myoclonic jerking 

➧ Photophobia 

➧ Visual disturbances: Periodic flashes of light, changes in the visual field, Visual snow, Restricted or "tunnel vision" 

➧ Visual, auditory, or other sensory hallucinations: 

-Warping or waving of surfaces and edges 

-Textured surfaces 

-"Dancing" lines; "spiders", insects

-Lifelike objects indistinguishable from reality 

-The hallucinated presence of people not actually there 

➧ Rarely: seizures, coma, and death 

➧ Orthostatic hypotension (sudden dropping of systolic blood pressure when standing up suddenly) and significantly increased risk of falls in the elderly population.

Treatment:

Central anticholinergic syndrome is completely reversible and subsides once all of the causative agents have been excreted.

Physostigmine:

➧ It is one of only a few drugs that can be used as an antidote for anticholinergic poisoning because it crosses BBB.

- Dose: 0.01-0.03 mg/kg IV, repeated after 15-30 min. If necessary. 

- Duration of action: about 30-60 min after intravenous IV injection.

- Side effects: nausea and vomiting, abdominal cramps, bradycardia, and hypotension

- Physostigmine was found to increase the risk of cardiac toxicity.

Nicotine:

➧ It counteracts anticholinergics by binding to the nicotinic acetylcholine receptors and activating them.

Caffeine:

➧ It is an adenosine receptor antagonist, that counteracts the anticholinergic symptoms by reducing sedation and increasing acetylcholine activity, thereby causing alertness and arousal.

➧ Caffeine can also inhibit acetylcholinesterase non-competitively.

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